Tokushima University / Educator and Researcher Directory --- Nakajima, Yukiko

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Tokushima University ⟩ University Hospital ⟩ Clinical Division ⟩ Department of General Dentistry ⟩ Periodontology and Endodontology ⟩
Tokushima University ⟩ Faculty of Dentistry ⟩ Course in Dentistry ⟩ Clinical Dentistry for Oral Health and Function ⟩ Periodontology and Endodontology ⟩

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Academic Paper (Judged Full Paper):

1.	Chie Wada -Mihara, Koji Naruishi, Mika Bandou, Yasufumi Nishikawa, Lew Jung-Hwan, Eijiro Sakamoto, Takahisa Ikuta, Kaoru Kono, Yukari Kajiura, Mari Hashimoto, Yukiko Nakajima, Yuji Inagaki, Masami Ninomiya, Jun-ichi Kido and Toshihiko Nagata : Post clinical clerkship-OSCEを見据えた歯周病科での模擬OSCEの概要, Journal of Oral Health and Biosciences, Vol.29, No.2, 49-53, 2017. (Tokushima University Institutional Repository) ● Metadata: 111059 (Link to Publication Site) ● Publication site (DOI): 10.20738/johb.29.2_49 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.20738/johb.29.2_49 (Tokushima University Institutional Repository: 111059, DOI: 10.20738/johb.29.2_49)
2.	Takahisa Ikuta, Yuji Inagaki, Kazuya Tanaka, Tsuyoshi Saito, Yukiko Nakajima, Mika Bandou, Jun-ichi Kido and Toshihiko Nagata : Gene polymorphism of β-defensin-1 is associated with susceptibility to periodontitis in Japanese., Odontology, Vol.103, No.1, 66-74, 2015. (Summary) Periodontitis is a multifactorial disease associated with genetic and environmental factors. Single-nucleotide polymorphisms (SNPs) are associated with susceptibility to common diseases such as diabetes and periodontitis. Although the oral cavity is exposed to various organisms, the conditions are well controlled by innate and acquired immune systems. Antimicrobial peptides (AMPs) play an important role in the innate immune system; however, the association of AMP-SNPs with periodontitis has not been fully elucidated. This study investigated the relationship between AMP-SNPs and periodontitis in Japanese. One hundred and five Japanese subjects were recruited, which included patients with aggressive, severe, moderate and mild periodontitis, and age-matched healthy controls. Genomic DNA was isolated from peripheral blood and genotypes of SNPs of β-defensin-1 and lactoferrin genes (DEFB1: rs1799946, rs1800972 and rs11362; and LTF: rs1126478) were investigated using the PCR-Invader assay. Protein level of AMPs in gingival crevicular fluid (GCF) was quantified by ELISA. Case-control studies revealed that the -44 CC genotype of DEFB1 (rs1800972) was associated with periodontitis (OR 2.51), particularly with severe chronic periodontitis (OR 4.15) and with combined severe and moderate chronic periodontitis (OR 4.04). No statistical differences were found in other genotypes. The β-defensin-1 concentrations in GCF were significantly lower in subjects with the -44 CC genotype of DEFB1 than in those without this genotype. No significant differences between GCF concentrations of AMPs and other genotypes were detected. The -44 CC genotype of the β-defensin-1 gene (DEFB1 rs1800972) may be associated with susceptibility to chronic periodontitis in Japanese. (Tokushima University Institutional Repository) ● Metadata: 106075 (Link to Publication Site) ● Publication site (DOI): 10.1007/s10266-013-0139-9 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24276427 ● Summary page in Scopus @ Elsevier: 2-s2.0-84887927465 (Tokushima University Institutional Repository: 106075, DOI: 10.1007/s10266-013-0139-9, PubMed: 24276427, Elsevier: Scopus)
3.	Yuji Inagaki, Yukiko Nakajima, Masumi Horibe, 生田貴久, Yukari Kajiura, Koji Naruishi, Jun-ichi Kido and Toshihiko Nagata : 肥満糖尿病ラット歯周炎の歯肉組織におけるオステオポンチンの局在, Journal of the Japanese Association of Periodontology, Vol.67, No.4, 149-158, 2015. (Link to Publication Site) ● Publication site (DOI): 10.2329/perio.57.149 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390001204416151552 ● Search Scopus @ Elsevier (DOI): 10.2329/perio.57.149 (DOI: 10.2329/perio.57.149, CiNii: 1390001204416151552)
4.	Yukiko Nakajima, Yuji Inagaki, Jun-ichi Kido and Toshihiko Nagata : Advanced glycation end-products increase expression of S100A8 and A9 via RAGE-MAPK in rat dental pulp cells, Oral Diseases, Vol.21, No.3, 328-334, 2015. (Summary) Advanced glycation end products (AGE) are involved in the progression of diabetic complications. Although our previous reports show that AGE increased dental pulp calcification, AGE accumulation is also associated with inflammation. This study examined AGE effect on the expression of inflammation factors using rat dental pulp tissues and cell cultures. Receptor for AGE (RAGE), S100A8, S100A9, and interleukin (IL)-1β were selected as inflammation parameters. Rat dental pulp cells were cultured and treated with AGE, and the effects were determined by real-time PCR. An anti-RAGE antibody or MAPK pathway inhibitors (PD98059, SB203580, and SP60012) were used to investigate AGE signaling pathway. The mRNA levels of RAGE, S100A8, S100A9, and IL-1β were higher in diabetic pulp tissues. AGE increased mRNA expressions of S100A8, S100A9, and IL-1β in cultured dental pulp cells. In the presence of anti-RAGE antibody, AGE did not increase in S100A8 or S100A9 expressions. The AGE-induced increases in S100A8 and S100A9 were inhibited by PD98059 and SB203580, respectively. Advanced glycation end products increased mRNA expression of S100A8, S100A9, and IL-1β under diabetic pulp conditions, and AGE-induced increases in S100A8 and S100A9 expressions may be associated with the RAGE-MAPK signaling pathway. (Keyword) Advanced Glycosylation End Product-Specific Receptor / Animals / Antibodies / Calgranulin A / Calgranulin B / Cells, Cultured / Dental Pulp / Diabetes Mellitus / Flavonoids / Gene Expression / Glycosylation End Products, Advanced / Imidazoles / Interleukin-1beta / MAP Kinase Signaling System / Male / Mitogen-Activated Protein Kinases / Pyridines / RNA, Messenger / Rats (Link to Publication Site) ● Publication site (DOI): 10.1111/odi.12280 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25098709 ● Summary page in Scopus @ Elsevier: 2-s2.0-84925124937 (DOI: 10.1111/odi.12280, PubMed: 25098709, Elsevier: Scopus)
5.	Yukiko Nakajima, Yuji Inagaki, Yuka Hiroshima, Jun-ichi Kido and Toshihiko Nagata : Advanced glycation end-products enhance calcification in cultured rat dental pulp cells, Journal of Endodontics, Vol.39, 873-878, 2013. (Summary) Amorphous calcification frequently appears in dental pulp tissues of diabetic patients; however, its pathologic process has not been fully elucidated. We previously found that pulp stones and thickened predentin occurred more frequently in diabetic rats. Recent findings demonstrated that accumulation of advanced glycation end-products (AGE) might be involved in vascular calcification complicated with diabetes. The aim of this study was to determine the effect of AGE on calcified nodule formation by rat dental pulp cells in culture. Rat dental pulp cells and gingival fibroblasts were independently cultured with 50 and 100 μg/mL AGE. Alkaline phosphatase activity and calcified nodule formation were measured. Expressions of receptor for AGE, osteopontin (OPN), and osteocalcin (OCN) mRNA were determined by quantitative real-time polymerase chain reaction. Protein levels of OPN and OCN secreted in culture medium were quantified by enzyme-linked immunosorbent assay. AGE (50 and 100 μg/mL) markedly increased both alkaline phosphatase activity and calcified nodule formation in dental pulp cells (P < .01), whereas it did not affect those in gingival fibroblasts. Real-time polymerase chain reaction analysis revealed that AGE increased mRNA expressions of receptor for AGE, OPN, and OCN in dental pulp cells (P < .05). Enzyme-linked immunosorbent assay analysis revealed that the protein levels of OPN and OCN produced by dental pulp cells were higher in AGE-treated than in untreated cells (P < .05). AGE enhanced the calcification potentials of rat dental pulp cells, suggesting that it may stimulate pathologic calcification of diabetic dental pulp tissues. (Keyword) Alkaline Phosphatase / Animals / Cell Culture Techniques / Cells, Cultured / Dental Pulp / Dental Pulp Calcification / Fibroblasts / Gingiva / Glycosylation End Products, Advanced / Male / Osteocalcin / Osteopontin / Rats / Rats, Wistar / Receptors, Immunologic / Time Factors (Link to Publication Site) ● Publication site (DOI): 10.1016/j.joen.2012.11.027 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23791254 ● Summary page in Scopus @ Elsevier: 2-s2.0-84879412695 (DOI: 10.1016/j.joen.2012.11.027, PubMed: 23791254, Elsevier: Scopus)

Academic Paper (Unrefereed Paper):

1.	Jun-ichi Kido, Mika Bandou, Yuji Inagaki, 生田貴久, Yukari Kajiura, Yukiko Nakajima, Eijiro Sakamoto, Chie Wada -Mihara, Masami Ninomiya, 西川泰史, Jung-Hwan Lew, Koji Naruishi and Toshihiko Nagata : Diagnosis of Periodontal Diseases using Biomarkers in Gingival Crevicular Fluid, Journal of Oral Health and Biosciences, Vol.29, No.1, 13-20, 2016. (Summary) Periodontal diseases cause an inflammation and degradation of periodontal tissues and missing of teeth. The incidence rate of periodontal diseases is high in middle-aged and elderly people.A reasonable diagnosis of periodontal diseases is very important to keep teeth, however, conventional examinations of periodontal diseases is not necessarily exact and objective. Gingival crevicular fluid (GCF) is an exudate secreted from periodontal tissues and contains many components including proteolytic enzymes, inflammatory cytokines, blood-associated proteins, cellular and bacterial fragments. Because some proteins in GCF are related to inflammation, tissue degradation and bone metabolism, those proteins have been studying as a diagnostic marker of periodontal diseases. GCF is noninvasively collected using a sterile paper strip and biomarkers are determined using enzyme-linked immunosorbent assay (ELISA) and enzyme activity assay. We identified calprotectin, an inflammationrelated protein, in GCF and calprotectin level in GCF from periodontitis sites was significantly higher than that of healthy control. Calprotectin level in GCF was positively correlated to gingival index and other biomarkers and decreased by periodontal treatments. Resistin is an adipocytokine and its level increases in some inflammatory diseases. Resistin level in GCF from periodontitis sites was high compared to the level of healthy control samples. Procollagen type I C-terminal peptide (PICP) is a biomarker for bone metabolism and its level was high in GCF collected from periodontitis sites. These results suggested that calprotectin, resistin and PICP are useful biomarkers for periodontal diseases. On the other hand, we showed that glycated albumin (GA), a marker of diabetes mellitus (DM), was contained in GCF and GA level in GCF from DM patients was significantly higher than that of non-DM individuals. Components in GCF may be biomarkers of systemic diseases as well as periodontal diseases and their determination will be useful diagnostic examination of some diseases. Recently, we have been studying the determining system of GCF calprotectin, including microchip ELISA, surface plasmon resonance assay and immuno-chromatography assay. When GCF biomarkers are determined using the determining systems, we will simply, exactly and objectively diagnose periodontal diseases at our dental offices. (Keyword) 歯周病診断 / バイオマーカー / 歯肉溝滲出液 (Tokushima University Institutional Repository) ● Metadata: 109875 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050845763956844416 (Tokushima University Institutional Repository: 109875, CiNii: 1050845763956844416)

Proceeding of International Conference:

1.	Yukari Kajiura, Koji Naruishi, Yukiko Nakajima, Yasufumi Nishikawa, Jung-Hwan Lew, Jun-ichi Kido and Toshihiko Nagata : High glucose enhaces P. gingivalis-induced cytokine production in THP-1 monocytes, 94th General Session & Exhibition, International Association for Dental Research, Seoul, Jun. 2016.
2.	Yukiko Nakajima, Jun-ichi Kido, Yuji Inagaki, Mika Bandou, Yuka Hiroshima, Hiromi Murata and Toshihiko Nagata : Effect of hypoxia on gene expression in human oral keratinocytes, 10th Asian Pacific Society of Periodontology Meeting, Nara, Sep. 2013.
3.	Jun-ichi Kido, Mika Bandou, Yuji Inagaki, Yuka Hiroshima, Hiromi Murata, Chie Wada -Mihara, 梶浦由加里, 生田貴久, 篠原宏貴, 橋本万里, Yukiko Nakajima, Yukiko Bandou, Makoto Funaki, Haruhiko Saito and Toshihiko Nagata : Diagnosis of diabetes-associated periodontitis using glycoalbumin and calprotectin in gingival crevicular fluid, 10th Asian Pacific Society of Periodontology Meeting, Nara, Sep. 2013.
4.	Yukiko Nakajima, Yuji Inagaki, Yuka Hiroshima, Jun-ichi Kido and Toshihiko Nagata : AGE induces calcification and inflammatory factors in dental pulp tissues, 91th General Session & Exhibition of the International Accociation for Dental Research, Seattle, USA, May 2013.

Proceeding of Domestic Conference:

1.	Masami Ninomiya, Yuji Inagaki, Chie Wada -Mihara, Mika Bandou, Yukiko Nakajima, Eijiro Sakamoto, Ikuta Takahisa, Nishikawa Yasufumi, Jung-Hwan Lew, Rie Kido, Takagi Ryousuke, Nonaka Kouhei, Koji Naruishi, Jun-ichi Kido and Toshihiko Nagata : 新規歯周組織再生剤「リグロス歯科用液キット」の有効性, 四国歯学会第51回例会, Jun. 2017. (Keyword) periodontitis / fibroblast growth factor 2 / periodontal regeneration / Regroth
2.	Chie Wada -Mihara, Koji Naruishi, Mika Bandou, 西川泰史, Hwan Jung Lew, Eijiro Sakamoto, 生田貴久, 河野薫, Yukari Kajiura, 橋本万里, Yukiko Nakajima, Yuji Inagaki, Masami Ninomiya, Jun-ichi Kido and Toshihiko Nagata : アドバンスドOSCEを見据えた当科の模擬OSCEの概要, Shikoku Dental Research, Vol.29, No.2, 49-53, Jun. 2017.
3.	美原智恵, Koji Naruishi, Mika Bandou, 西川泰史, Jung-Hwan Lew, Eijiro Sakamoto, 生田貴久, 河野薫, Yukari Kajiura, 橋本万里, Yukiko Nakajima, Yuji Inagaki, Masami Ninomiya, Jun-ichi Kido and Toshihiko Nagata : アドバンスOSCEを見据えた当科の模擬OSCEの概要, 第49回四国歯学会例会, Jun. 2016.
4.	Jun-ichi Kido, Mika Bandou, Yukiko Nakajima, Yukari Kajiura, Yuji Inagaki, 生田貴久, Eijiro Sakamoto, Koji Naruishi and Toshihiko Nagata : ヒト口腔上皮細胞と歯肉線維芽細胞において低酸素環境が誘導する遺伝子発現の比較, 第143回日本歯科保存学会秋季学術大会, Nov. 2015.
5.	Yukari Kajiura, Jun-ichi Kido, Yukiko Nakajima, Mika Bandou, Yuji Inagaki, Koji Naruishi, Eijiro Sakamoto, Kaori Abe, Yuka Hiroshima and Toshihiko Nagata : 低酸素環境が誘導するヒト口腔上皮細胞における遺伝子発現の解析, 第58回秋季日本歯周病学会学術大会, Sep. 2015.
6.	Mika Bandou, Yukari Kajiura, Yukiko Nakajima, Jun-ichi Kido, Yuji Inagaki, Hiromi Murata and Toshihiko Nagata : 最終糖化産物は口腔由来線維芽細胞・上皮細胞での炎症関連因子と酸化ストレス因子の発現に影響する, 第57回秋季日本歯周病学会学術大会, Oct. 2014.
7.	Yukari Kajiura, Yukiko Bandou, Jun-ichi Kido, Mika Bandou, Yuji Inagaki, Yukiko Nakajima, 生田貴久, Hiromi Murata, Yuka Hiroshima, Koji Naruishi and Toshihiko Nagata : 歯周病および糖尿病患者の歯肉溝滲出液中のYKL-40レベルの検討, 第57回秋季日本歯周病学会学術大会, Oct. 2014.
8.	Jun-ichi Kido, Yukiko Nakajima, Mika Bandou, Yuji Inagaki and Toshihiko Nagata : 低酸素環境とP.gingivalis由来リポ多糖はヒト口腔上皮細胞での炎症関連因子および血管関連因子の発現を調節する, 第140回日本歯科保存学会春季学術大会, Jun. 2014.
9.	Yukari Kajiura, Mika Bandou, Jun-ichi Kido, Yuji Inagaki, 生田貴久, 橋本万里, 篠原宏貴, Masami Ninomiya, Hiromi Murata, Yukiko Nakajima, Satoshi Yoneda, 美原智恵, Yuka Hiroshima, Keiji Oishi and Toshihiko Nagata : 歯肉溝滲出液中のグリコアルブミンおよびカルプロテクチンを指標とした糖尿病関連歯周炎の診断, 第57回春季日本歯周病学会学術大会, May 2014.
10.	Yukiko Nakajima, Jun-ichi Kido, Mika Bandou, Yuji Inagaki and Toshihiko Nagata : Effect of hypoxia and P. gingivalis-lipopolysaccharide on the expression of inflammation-related molecules in human oral keratinocytes, 第57回春季日本歯周病学会学術大会, May 2014.
11.	Mika Bandou, Yukiko Nakajima, Yukari Kajiura, Jun-ichi Kido, Yuji Inagaki, Hiromi Murata and Toshihiko Nagata : 最終糖化産物は歯周組織細胞での炎症性関連因子と酸化ストレス因子の発現に影響する, 第57回日本糖尿病学会年次学術集会, May 2014.
12.	Yukari Kajiura, Yukiko Bandou, Jun-ichi Kido, Mika Bandou, Yuji Inagaki, Yukiko Nakajima, 生田貴久, Hiromi Murata, Yuka Hiroshima, Koji Naruishi and Toshihiko Nagata : 歯周病および糖尿病患者の歯肉溝滲出液中のYKL-40レベルの検討, 第57回日本歯周病学会秋期学術大会抄録集, May 2014.
13.	生田貴久, Yuji Inagaki, Yukiko Nakajima, Mika Bandou, Jun-ichi Kido and Toshihiko Nagata : 日本人歯周病患者を対象とした抗菌ペプチド遺伝子のSNPs解析と疾患感受性の検討, 第139回日本歯科保存学会秋季学術大会, Oct. 2013.
14.	Yukiko Nakajima, Jun-ichi Kido, Yuji Inagaki, Mika Bandou, Yuka Hiroshima, Hiromi Murata and Toshihiko Nagata : 低酸素環境がヒト口腔上皮細胞の各種遺伝子発現に及ぼす影響, 第56回秋季日本歯周病学会学術大会, Sep. 2013.
15.	Yukiko Nakajima, Yuji Inagaki, Jun-ichi Kido and Toshihiko Nagata : 最終糖化産物(AGE)はRAGE-MAPK経路を介してラット培養歯髄細胞の石灰化物形成を促進する, 第138回日本歯科保存学会春季学術大会, Jun. 2013.

Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)

Analysis of the disorder on cell function induced by advanced glycation end-product (AGE) in dental pulp, gingival and alveolar bone tissues (Project/Area Number: 15K15701 )
糖尿病関連歯周炎におけるHMGB1-RAGEの役割 (Project/Area Number: 26861818 )
Search by Researcher Number (70709526)